Acrolein-mediated neurotoxicity in growing Wistar male rats

https://doi.org/10.1016/j.pestbp.2018.05.006Get rights and content

Highlights

  • Acrolein caused neurofilament accumulation in brain tissue.

  • Acrolein mediated histopathological changes were observed in brains of male rats.

  • GFAP and MBP levels were not changed by acrolein exposure.

Abstract

Acrolein is an environmental and food contaminant widely produced by thermal processed organic compounds. It can be used as a biocide and is known to be generated endogenously by lipid peroxidation. This study was designed for evaluating acrolein toxicity in the context of GFAP, MBP, neurofilaments and histological examination of brain tissues and also hematological paremeters in pubertal male rats. 3–4 weeks aged Wistar male rats were exposed to 0.5, 1 and 2 mg/kg/day acrolein for 90 days. According to acrolein exposure results, slight changes observed in hematological parameters, however no significant differences were observed in GFAP and MBP. Unlikely, acrolein caused several histopathological changes in brain tissues as well as neurofilament accumulation. It may be concluded that acrolein might contribute to formation of neurodegenerative disorders.

Section snippets

Introductıon

Acrolein, a highly electrophilic α,β-unsaturated aldehyde, is an environmental and food contaminant widely produced by thermal processed organic compounds including carbohydrates, amino acids and fats [1,2]. Human exposure to acrolein may occur via endogenously, diet or environmental sources such as oil-fried foods, tobacco smoke, incomplete combustion of plastic, wood and petrol [1,3]. Acrolein occurence was reported in foods, fruits and beverages such as raw cocoa beans, vegetable oils, white

Animals and experimental design

This study was set up to evaluate subchronic effects of orally administrated acrolein in terms of hematological, biochemical, histopathological and immunohistochemical analysis in growing Wistar male rats. 3–4 weeks aged Wistar male rats were provided from Production Center of Experimental Animals with the approval of Animal Experimentations Local Ethic Commitee of Hacettepe University. Rats were acclimatized for a week to our laboratory conditions, maintained in a temperature and humidity

Body weights, food and water consumption

According to results, acrolein treatment caused several changes in mean body weight gains. Body weight gains and percentage of body weight gains in 1 and 2 mg/kg/day acrolein treatment groups decreased statistically in response to acrolein exposure compared to control group (respectively, P = 0.0125; P = 0.0057). Food and water consumptions were not altered in all groups although water consumption increased in 0.5 mg/kg/day acrolein group, it was not statistically significant. Body weight gains

Discussion

In recent years, increase in central nervous system disorders is a major health problem. It is noteworthy that over 1 billion people worldwide have central nervous system disorders [21]. Among the central nervous system disorders, neurodegenerative diseases are the most engrossing resulting in identified by relatively age dependent decrease in neurological functions and accompanied by neuronal damage [21]. Although much of the neurodegenerative disorders are known to be age-related, recent

Acknowledgement

We thank to Hacettepe University Scientific Projects Coordination Unit (Project No: 010D08601008) for the financial support. This research is a MSc thesis of Gökçen Mülayimçelik Özgün.

References (41)

  • J.B. Angevine

    Nervous system, organization of A2

  • J. Middeldorp et al.

    GFAP in health and disease

    Prog. Neurobiol.

    (2011)
  • Z. Yang et al.

    Glial fibrillary acidic protein: from intermediate filament assembly and gliosis to neurobiomarker

    Trends Neurosci.

    (2015)
  • J.F. Stevens et al.

    Acrolein: sources, metabolism, and biomolecular interactions relevant to human health and disease

    Mol. Nutr. Food Res.

    (2008)
  • X. Liu et al.

    Acute acrolein exposure induces impairment of vocal fold epithelial barrier function

    PLoS ONE

    (2016)
  • O. Faroon et al.

    Acrolein environmental levels and potential for human exposure

    Toxicol. Ind. Health

    (2008)
  • G. Aldini et al.

    Protein modification by acrolein: relevance to pathological conditions and inhibition by aldehyde sequestering agents

    Mol. Nutr. Food Res.

    (2011)
  • N.Y. Calingasan et al.

    Protein-bound Acrolein

    J. Neurochem.

    (1999)
  • J.P. Kehrer et al.

    The molecular effects of acrolein

    Toxicol. Sci.

    (2000)
  • Y.-T. Wang et al.

    Acrolein acts as a neurotoxin in the nigrostriatal dopaminergic system of rat: involvement of α-synuclein aggregation and programmed cell death

    Sci. Rep. UK

    (2017)
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